Greenhouse gasses from cars, trucks,and busses are less than what results from animal agriculture.A United Nations Food and Agriculture Organization report published in 2006 points the finger at livestock operations globally. The study asserts that a 50% decrease must be achieved in order to avoid increasing the current level of environmental damage.
Animal farms around the world generate 18% more greenhouse emissions than all of the previously mentioned transportaion methods combined. Further, livestock production currently occupies 30 percent of earths land surface. The areas used for grazing are a major source of deforestation, particularly in Latin America, where 70% of former forest lands are used for grazing.
By far the most important non-CO2 greenhouse gas is methane, and the number one source of methane worldwide is animal agriculture.[1]
Methane is responsible for nearly as much global warming as all other non-CO2 greenhouse gases put together.[2] Methane is 21 times more powerful a greenhouse gas than CO2.[3] While atmospheric concentrations of CO2 have risen by about 31% since pre-industrial times, methane concentrations have more than doubled.[4] Whereas human sources of CO2 amount to just 3% of natural emissions, human sources produce one and a half times as much methane as all natural sources.[5] In fact, the effect of our methane emissions may be compounded as methane-induced warming in turn stimulates microbial decay of organic matter in wetlands—the primary natural source of methane.[6]
With methane emissions causing nearly half of the planet’s human-induced warming, methane reduction must be a priority. Methane is produced by a number of sources, including coal mining and landfills—but the number one source worldwide is animal agriculture.[7] Animal agriculture produces more than 100 million tons of methane a year.[8] And this source is on the rise: global meat consumption has increased fivefold in the past fifty years, and shows little sign of abating.[9] About 85% of this methane is produced in the digestive processes of livestock,[10] and while a single cow releases a relatively small amount of methane,[11] the collective effect on the environment of the hundreds of millions of livestock animals worldwide is enormous. An additional 15% of animal agricultural methane emissions are released from the massive “lagoons” used to store untreated farm animal waste,[1] and already a target of environmentalists’ for their role as the number one source of water pollution in the U.S.[13]
The conclusion is simple: arguably the best way to reduce global warming in our lifetimes is to reduce or eliminate our consumption of animal products. Simply by shifting to a plant-based diet[14][15][16] we can eliminate one of the major sources of emissions of methane, the greenhouse gas responsible for almost half of the global warming impacting the planet today.
1. Animal agriculture is also a major source of nitrous oxide emissions, another important greenhouse gas 310 times more powerful than carbon dioxide. 73% of U.S. emissions of nitrous oxide come from animal grazing, manure management, and crop growing practices—with half of U.S. crops grown for livestock feed. Agricultural emissions of nitrous oxide in the U.S. increased 9% from 1990 to 2002. “Inventory of U.S. Greenhouse Gas Emissions: 1990-2002,” EPA 430-R-04-003, U.S. Environmental Protection Agency, 15 April 2004, p. ES-16, http://www.epa.gov/globalwarming/publications/ emissions.
2. Hansen and Sato, supra note 11. Estimated climate forcing of methane from 1850 to 2000 is 0.7 W/m2, while estimated forcing of CFCs, tropospheric ozone, and nitrous oxide combined is 0.9 W/m2.
3. “Global Warming Potentials”, supra note 10.
4. Atmospheric CO2 concentrations have risen from 278 parts per million (ppm) in 1750 to 365 ppm in 1998. Atmospheric concentrations of methane have increased by 149% since 1750, from .700 ppm to 1.745 ppm. “Emissions of Greenhouse Gases in the United States 2002”, Chapter 1, Energy Information Administration, U.S. Department of Energy, October 2003, http://www.eia.doe.gov/oiaf/1605/ggrpt.
5. Natural sources emit 770 billion metric tons of CO2, and 239 million metric tons of methane, compared to 23.1 billion and 359 million, respectively, for anthropogenic sources. “Emissions of Greenhouse Gases in the United States 2002”, supra note 20.
6. Hansen, et al, supra note 5. It is also possible that warming may dampen natural sources of methane by drying out wetlands.
7.Animal agriculture is responsible for 32% of global methane emissions from human activity, including 28% from domesticated livestock and 4% from livestock manure. Natural gas is the second largest source, accounting for 15% of emissions. Kruger, Dina, “The Role of ‘Other Gases’ in Addressing Climate Change”, U.S. Environmental Protection Agency, 12 Feb 2004, http://www.iges.or.jp/en/cp/ output_all/workshop/usjapan/pdf/06Kruger.pdf.
8. “Emissions of methane from livestock”, Climate Change Fact Sheet 32, Information Unit on Climate Change (IUCC), UNEP, 1 May 1993, http://www.unep.ch/iucc/fs032.htm.
9. World meat production reached 242 million tons in 2002, from 122 million tons in 1977, and from 44 million tons in 1950. Additionally, per capita meat consumption has more than doubled since 1950, from 17 to 39 kg per person. Vital Signs 2003, Worldwatch Institute, May 2003, p.30-31, http://www.worldwatch.org/pubs/vs/2003. The majority of the meat is consumed by developed countries. Delgado, Christopher et al., Livestock to 2020: The Next Food Revolution, “Food, Agriculture, and the Environment Discussion Paper 28”, International Food Policy Research Institute, May 1999, http://www.ifpri.org/2020/dp/dp28.pdf.
10. “The Role of ‘Other Gases’ in Addressing Climate Change”, supra note 23. Methane emissions come particularly from ruminant animals, like cows, sheep, buffalo, and goats, but also from non-ruminants like pigs and horses. “Emissions of methane from livestock”, supra note 24.
11.Not including methane released from manure, an adult cow produces 80-110 kg of methane a year. “Frequent Questions”, Ruminant Livestock, U.S. Environmental Protection Agency, http://www.epa.gov/rlep/faq.html.
12.“The Role of ‘Other Gases’ in Addressing Climate Change”, supra note 23.
13.“Water Quality Conditions in the United States”, U.S. Environmental Protection Agency, August 2002, http://www.epa.gov/305b/2000report.
14.Herein, the term “vegetarian” is used to refer not just to a meatless diet, but to one free of animal products, i.e. a “vegan” diet. Dairy cows, for example, produce even more methane per animal than beef cattle. Logically, the same concerns extend beyond diet to the consumption of other consumer goods derived from livestock, like wool and leather.
15.Because ruminant livestock produce far more methane than non-ruminant livestock, reductions in agricultural methane can also be achieved by shifting consumption away from cows and sheep in favor of chickens and pigs. However, the benefits of such shifts are not simple; for example, in the U.S., manure from pigs produces more than five times as much methane as manure from beef cattle. (“Inventory of U.S. Greenhouse Gas Emissions: 1990-2002”, p. 181, supra note 17.) Moreover, the large scale production of these animals in concentrated animal feeding operations (CAFOs) is associated with numerous other environmental harms already extensively documented by environmental organizations, making the trade of one environmental danger for another a Faustian bargain.
16.The U.S. Environmental Protection Agency’s efforts to address methane from livestock amount to encouraging changes in feed and increasing the amount of product (meat, milk, offspring) per animal. Even at best such efforts are unlikely to achieve large reductions in emissions per animal, and any such reductions are easily swamped by increases in the number of animals raised overall. Methane emissions from manure can also be captured and used to produce energy.
Thursday, March 29, 2007
Thursday, March 22, 2007
Lose Weight by Eating More Dairy?...Maybe Not So Fast
Dairy Diet Myth
You’ve probably seen the ads in magazines or on TV. “Milk, cheese-
yogurt. Burn more fat, lose weight.” Drink 24 ounces
of milk every 24 hours and that skinny hourglass figure will be
yours. Eat three servings of yogurt every day and squeeze into
that itsy-bitsy bikini...
Beginning October 2003 "Drink Milk... Lose Weight" ads ran in over 30 newspapers and magazines when the dairy industry launched an entire "Healthy Weight with Milk" campaign to boost sales. Curiously, that also happened to be the same year a review of that exact subject was published in the Journal of Nutrition. The review found nine randomized controlled studies in the medical literature on body weight and dairy. Seven of the nine studies found no significant change in body weight compared to controls and the last two found that those who increased their dairy consumption gained significantly more weight than the nondairy control groups.[1] Subsequent and even larger studies published in 2004[2] and 2005[3] showed the exact same thing.
So, wait a second. How can the dairy industry's ads claim that "a clinical study shows it helps you burn more fat and lose more weight than just cutting calories alone?" Well, because there are actually three small published studies that found greater weight loss in people who were told to cut calories and eat dairy foods and all were done by one researcher with a patent on the claim. Michael Zemel of the University of Tennessee, found that study participants instructed to eat more dairy did seem to lose more weight. Yes, of course the studies were bought and paid for by the dairy industry, but it goes further than that. This guy Zemel owns a patent on the claim that dairy foods aid weight loss, which is licensed to dairy food manufacturers. As the Center for Science in the Public Interest noted, "In the world of patents and PR, a little science can go a long way."[4] For an in depth analysis of Zemels work and how it is assisting the Dairy Industry check out the Nutrition Action Health Letter Spetember 2005 available online at cspinet.org
Similar maneuverings were involved in the increased dairy recommendation in the new USDA Dietary Guidelines, even though a recent World Health Organization review found no significant relationship at all between low dairy consumption and osteoporotic fracture risk.[5] Assigned to write the dairy guideline was Connie Weaver, head of nutrition at Purdue University and a funding favorite of the National Dairy Council. Walter Willet, head of nutrition at Harvard, calls the guideline committee's report "egregious," accusing them of ignoring the evidence linking dairy to cancer. "There is no nutritional requirement for dairy," Dr. Willet told the Wall Street Journal, "at all."[6]
To hopefully clear up the dairy/weight question once and for all, on June 6, 2005, Harvard researchers published what may be considered the definitive study on the subject in the Archives of Pediatrics and Adolescent Medicine. A study which followed the milk-drinking habits of not 11 kids, or even 12 kids, but over 12,000 kids! After following these 9- though 14-year-olds for years, they found that "children who reported higher total milk intake experienced larger weight gains." The more milk they drank, the heavier they became. Boys who drank the "recommended" three servings of milk a day were 35% more likely to become overweight and girls who drank three servings were 36% more likely to become overweight over time.[7]
"Given the high prevalence of lactose intolerance, the energy content and saturated fat in milk, and evidence that dairy products may promote both male (prostate) and female (ovarian) cancers, we should not assume that high intakes [of dairy] are beneficial," the researchers told reporters. "Furthermore, these cancers may be linked to consumption during adolescence."[8]
What most surprised the researchers was that those who drank low-fat milk (skim and 1%) gained the most weight of all! The weight gain seemed tied more to the dairy protein intake than the dairy fat intake (extra whey protein is often added to low-fat milk during processing). Although there are at least four human studies that show that the dairy protein whey itself may promote weight gain, the researchers guessed that the blame lay in the growth hormones in milk, like the sex steroid estrone found in whey. After all, milk is designed by mother nature to start an 80-pound calf on her way to 1,400 pounds by her second birthday.
This new study has serious implications for our childhood obesity epidemic, which not only has devastating health consequences but social consequences as well. A study released the same week by researchers at the Centers for Disease Control found that teens who perceived themselves as overweight were more than twice as likely to attempt suicide.[9]
[1] Barr SI. "Increased Dairy Product or Calcium Intake: Is Body Weight or Composition Affected in Humans?" Journal of Nutrition 133(2003):245-8S.
[2] Obesity Research 12(2004):A23.
[3] Gunther CW, Legowski PA, Lyle RM, et al. "Dairy Products Do Not Lead to Alterations in Body Weight or Fat Mass in Young Women In A 1-Y Intervention." Am J Clin Nutr 2005;81:751-6.
[4] "Dairy Does Diets." Nutrition Action Healthletter September 2004:8.
[5] Kanis JA, et al."A Meta-Analysis of Milk Intake and Fracture Risk: Low Utility For Case Finding." Osteoporisis International 21 October 2004.
[6] Zamiska N. "How Milk Got a Major Boost By Food Panel." Wall Street Journal 30 August 2004:B1.
[7] Berkey CS, et al. "Milk, Dairy Fat, Dietary Calcium, and Weight Gain ." Archives of Pediatrics and Adolescent Medicine 1599(2005):543-50.
[8] Fox M. "Milk may make for heavier kids, study finds." Reuters 6 June 2005.
[9] Eaton DK, et al. "Associations of Body Mass Index and Perceived Weight With Suicide Ideation and Suicide Attempts Among US High School Students." Archives of Pediatrics and Adolescent Medicine 1599(2005):513-9.
You’ve probably seen the ads in magazines or on TV. “Milk, cheese-
yogurt. Burn more fat, lose weight.” Drink 24 ounces
of milk every 24 hours and that skinny hourglass figure will be
yours. Eat three servings of yogurt every day and squeeze into
that itsy-bitsy bikini...
Beginning October 2003 "Drink Milk... Lose Weight" ads ran in over 30 newspapers and magazines when the dairy industry launched an entire "Healthy Weight with Milk" campaign to boost sales. Curiously, that also happened to be the same year a review of that exact subject was published in the Journal of Nutrition. The review found nine randomized controlled studies in the medical literature on body weight and dairy. Seven of the nine studies found no significant change in body weight compared to controls and the last two found that those who increased their dairy consumption gained significantly more weight than the nondairy control groups.[1] Subsequent and even larger studies published in 2004[2] and 2005[3] showed the exact same thing.
So, wait a second. How can the dairy industry's ads claim that "a clinical study shows it helps you burn more fat and lose more weight than just cutting calories alone?" Well, because there are actually three small published studies that found greater weight loss in people who were told to cut calories and eat dairy foods and all were done by one researcher with a patent on the claim. Michael Zemel of the University of Tennessee, found that study participants instructed to eat more dairy did seem to lose more weight. Yes, of course the studies were bought and paid for by the dairy industry, but it goes further than that. This guy Zemel owns a patent on the claim that dairy foods aid weight loss, which is licensed to dairy food manufacturers. As the Center for Science in the Public Interest noted, "In the world of patents and PR, a little science can go a long way."[4] For an in depth analysis of Zemels work and how it is assisting the Dairy Industry check out the Nutrition Action Health Letter Spetember 2005 available online at cspinet.org
Similar maneuverings were involved in the increased dairy recommendation in the new USDA Dietary Guidelines, even though a recent World Health Organization review found no significant relationship at all between low dairy consumption and osteoporotic fracture risk.[5] Assigned to write the dairy guideline was Connie Weaver, head of nutrition at Purdue University and a funding favorite of the National Dairy Council. Walter Willet, head of nutrition at Harvard, calls the guideline committee's report "egregious," accusing them of ignoring the evidence linking dairy to cancer. "There is no nutritional requirement for dairy," Dr. Willet told the Wall Street Journal, "at all."[6]
To hopefully clear up the dairy/weight question once and for all, on June 6, 2005, Harvard researchers published what may be considered the definitive study on the subject in the Archives of Pediatrics and Adolescent Medicine. A study which followed the milk-drinking habits of not 11 kids, or even 12 kids, but over 12,000 kids! After following these 9- though 14-year-olds for years, they found that "children who reported higher total milk intake experienced larger weight gains." The more milk they drank, the heavier they became. Boys who drank the "recommended" three servings of milk a day were 35% more likely to become overweight and girls who drank three servings were 36% more likely to become overweight over time.[7]
"Given the high prevalence of lactose intolerance, the energy content and saturated fat in milk, and evidence that dairy products may promote both male (prostate) and female (ovarian) cancers, we should not assume that high intakes [of dairy] are beneficial," the researchers told reporters. "Furthermore, these cancers may be linked to consumption during adolescence."[8]
What most surprised the researchers was that those who drank low-fat milk (skim and 1%) gained the most weight of all! The weight gain seemed tied more to the dairy protein intake than the dairy fat intake (extra whey protein is often added to low-fat milk during processing). Although there are at least four human studies that show that the dairy protein whey itself may promote weight gain, the researchers guessed that the blame lay in the growth hormones in milk, like the sex steroid estrone found in whey. After all, milk is designed by mother nature to start an 80-pound calf on her way to 1,400 pounds by her second birthday.
This new study has serious implications for our childhood obesity epidemic, which not only has devastating health consequences but social consequences as well. A study released the same week by researchers at the Centers for Disease Control found that teens who perceived themselves as overweight were more than twice as likely to attempt suicide.[9]
[1] Barr SI. "Increased Dairy Product or Calcium Intake: Is Body Weight or Composition Affected in Humans?" Journal of Nutrition 133(2003):245-8S.
[2] Obesity Research 12(2004):A23.
[3] Gunther CW, Legowski PA, Lyle RM, et al. "Dairy Products Do Not Lead to Alterations in Body Weight or Fat Mass in Young Women In A 1-Y Intervention." Am J Clin Nutr 2005;81:751-6.
[4] "Dairy Does Diets." Nutrition Action Healthletter September 2004:8.
[5] Kanis JA, et al."A Meta-Analysis of Milk Intake and Fracture Risk: Low Utility For Case Finding." Osteoporisis International 21 October 2004.
[6] Zamiska N. "How Milk Got a Major Boost By Food Panel." Wall Street Journal 30 August 2004:B1.
[7] Berkey CS, et al. "Milk, Dairy Fat, Dietary Calcium, and Weight Gain ." Archives of Pediatrics and Adolescent Medicine 1599(2005):543-50.
[8] Fox M. "Milk may make for heavier kids, study finds." Reuters 6 June 2005.
[9] Eaton DK, et al. "Associations of Body Mass Index and Perceived Weight With Suicide Ideation and Suicide Attempts Among US High School Students." Archives of Pediatrics and Adolescent Medicine 1599(2005):513-9.
Wednesday, March 14, 2007
Pills or Papayas? Survey Finds Americans Want Healthful Foods, Not More Medicines.
Sixty-Nine Percent of Respondents Would Prefer to Treat Diabetes with Dietary Changes, Such as a plant-based diet, Rather than Medication; Findings Reinforce Clinical Research Outlined in New Book
WASHINGTON--If you thought Americans would rather pop a pill to treat illness than make major diet changes, think again. A new survey shows the vast majority would rather change their diets—including trying a vegetarian diet—than use medicines. According to a nationally representative survey of 1,022 adults conducted in mid-January by Opinion Research Corporation, 69 percent of Americans would prefer to try a dietary approach. Just 21 percent preferred treating diabetes with medicines.
The survey, commissioned by the Physicians Committee for Responsible Medicine (PCRM), reinforces results from PCRM’s clinical research on diabetes, which has consistently found that people with diabetes adapt well to low-fat plant-based diets and gain important health benefits.
In Dr. Neal Barnard’s Program for Reversing Diabetes, a new book published in January 2007, PCRM president Neal Barnard, M.D., outlines a dietary approach to diabetes based on scientific research showing that a low-fat plant-based diet can lower high blood sugar levels three times more effectively than oral medications. In the past, many clinicians have felt that patients lack the willpower to make diet changes and would rather “pop a pill.” The new results show just the opposite.
“A low-fat plant-based diet offers a powerful way to control and even reverse diabetes,” said Dr. Barnard. “The idea that Americans would rather take pills than make diet changes is a myth. Americans clearly favor tackling serious diabetes with diet changes, including vegetarian diets.” The survey was conducted January 12 through 15 2007 and included 515 women and 507 men, 18 years and older, living in the continental United States.
Other key survey findings:
* Women are even more likely than men to prefer food changes over pills. Women preferred diet by 73 percent versus 17 percent for medicines. For men, the split was 65 percent versus 26 percent.
* People with more education and higher incomes were especially likely to favor a diet approach.
* Americans aged 45 to 64 were more enthusiastic about diet changes, compared with older Americans; 76 percent of the middle-aged respondents preferred diet changes. Among those aged 65 and above, the figure dropped slightly, to 59 percent. The most pill-happy generation was the 18- to 24-year-olds. But even in this group, only 30 percent favored using medicines, while 63 percent favored diet changes.
* People living in Western states were especially likely to prefer diet changes: 73 percent versus only 17 percent for drugs.
For detailed survey results or more information about Dr. Barnard’s book, contact Jeanne Stuart McVey at 202-686-2210, ext. 316, or jeannem@pcrm.org, or Simon Chaitowitz at 202-686-2210, ext. 309, or schaitowitz@pcrm.org.
WASHINGTON--If you thought Americans would rather pop a pill to treat illness than make major diet changes, think again. A new survey shows the vast majority would rather change their diets—including trying a vegetarian diet—than use medicines. According to a nationally representative survey of 1,022 adults conducted in mid-January by Opinion Research Corporation, 69 percent of Americans would prefer to try a dietary approach. Just 21 percent preferred treating diabetes with medicines.
The survey, commissioned by the Physicians Committee for Responsible Medicine (PCRM), reinforces results from PCRM’s clinical research on diabetes, which has consistently found that people with diabetes adapt well to low-fat plant-based diets and gain important health benefits.
In Dr. Neal Barnard’s Program for Reversing Diabetes, a new book published in January 2007, PCRM president Neal Barnard, M.D., outlines a dietary approach to diabetes based on scientific research showing that a low-fat plant-based diet can lower high blood sugar levels three times more effectively than oral medications. In the past, many clinicians have felt that patients lack the willpower to make diet changes and would rather “pop a pill.” The new results show just the opposite.
“A low-fat plant-based diet offers a powerful way to control and even reverse diabetes,” said Dr. Barnard. “The idea that Americans would rather take pills than make diet changes is a myth. Americans clearly favor tackling serious diabetes with diet changes, including vegetarian diets.” The survey was conducted January 12 through 15 2007 and included 515 women and 507 men, 18 years and older, living in the continental United States.
Other key survey findings:
* Women are even more likely than men to prefer food changes over pills. Women preferred diet by 73 percent versus 17 percent for medicines. For men, the split was 65 percent versus 26 percent.
* People with more education and higher incomes were especially likely to favor a diet approach.
* Americans aged 45 to 64 were more enthusiastic about diet changes, compared with older Americans; 76 percent of the middle-aged respondents preferred diet changes. Among those aged 65 and above, the figure dropped slightly, to 59 percent. The most pill-happy generation was the 18- to 24-year-olds. But even in this group, only 30 percent favored using medicines, while 63 percent favored diet changes.
* People living in Western states were especially likely to prefer diet changes: 73 percent versus only 17 percent for drugs.
For detailed survey results or more information about Dr. Barnard’s book, contact Jeanne Stuart McVey at 202-686-2210, ext. 316, or jeannem@pcrm.org, or Simon Chaitowitz at 202-686-2210, ext. 309, or schaitowitz@pcrm.org.
Thursday, March 8, 2007
California Dairy Giant Rejects Hormone Treated Milk
Consumer groups and public health organizations give cheers to California’s dairy industry after the Associated Press, along with other news agencies, reported yesterday that members of the largest dairy cooperative in California will be required to supply milk that is free of the hormone RBST. California Dairies Company's 650 members produce approximately 40% of California's milk and 10% of the nation's. By August First, they'll have to stop injecting their herds with the genetically engineered hormone or pay a premium for the co-op to truck their milk to other markets.
The industry wide shockwaves expected will assist in bringing US production regulations closer to that of our trading partners. In Europe and Canada US dairy exports recently have faced increasing resistance because of the refusal by American producers to discontinue using the hormone. European and Canadian authorities banned the hormone, recognize RBST as a threat to human health and have linked it to cancer. Several years ago documents came to public attention that showed Monsanto lied about their studies in order to gain approval from the FDA. The evidence on this is stunning and I have included an exhaustive list of references and hope that everyone gives them at least a quick glance.[1-58]
The good news for the consumers and the cows is not in any case good news for Monsanto, they are going to lose billions of dollars. Monsanto is the only supplier of the hormone, sold under the name Posilac, and sales have been estimated at close to $300 million annually, although Monsanto refuses disclosure of actual figures. Monsanto Corporation, in case anyone has forgotten, is that esteemed member of the American corporate community that has brought us such wonders as Agent Orange, Roundup and is the world's leader in GMO's (genetically modified organism).
RBST or Posilac is also an excellent example of corporate welfare. Posilac causes cows to produce more milk. So... what is wrong with that you ask? American taxpayers pay farmers not to produce milk and have been doing so for years. [59] There is an excess of dairy products in this country and our government buys it using our money. They buy it to keep the prices stable. If the supply exceeds demand, the price of dairy drops. The government steps in and keeps product from reaching the market. It ends up in government warehouses where much of it is simply thrown away. This is where “government cheese” came from. What is not eaten by our poor, elderly, and native populations ends up in the trash. Do you think that Monsanto cares about the fact that their product is contributing to this? I think Monsanto sees the bottom line.
The trouble with this continues because not only has Posilac been recognized as a human health threat, but so is the milk it helps produce more of! Dairy proteins and fats have been linked to heart disease, stroke [60,6], cancer [62-66], diabetes (types 1&2) [67,68], multiple sclerosis, arthritis, Crohn’s disease, irritable bowl syndrome, fibromyalgia, osteoporosis [69-78], and more. So where did Monsanto get the bright idea for such a great product? Since great minds think alike, maybe it was a friend of one of Monsanto’s other top executives; Donald Rumsfeld was a CEO for Monsanto. Hmmmm.
My hat is off to the California dairy producers for standing up to Monsanto and their money grubbing schemes regardless of the reason. It is a rare day when I have anything positive to say about the dairy industry, today just happens to be one of them.
References
1. Conyers, John. Letter to Richard R. Kusserow, Inspector General, Department of
Health and Human Services. May 9, 1990.
2. Kennelly J & DeBoer G. Bovine somatotropin. In Proceedings of the Alberta Dairy Seminar. Banff, Alberta, March 9-11, 1998.
3. Baer RJ, et al. Composition and flavor of milk produced by cows injected with recombinant bovine somatotropin. Journal of Dairy Science 72:1424-1434, 1989.
4. Capuco, AV et al. Somatotropin increases thyroxine-5’-monodeiodinase activity in lactating mammary tissue of the cow. Journal of Endocrinology 121(2):205-211, 1989.
5. Epstein, SS. Potential public health hazards of biosynthetic milk hormones.
International Journal of Health Services 20:73-84, 1990.
6. Kronfeld, DS. Safety of bovine growth hormone. Science 251:256-257, 1991.
7. U.S. General Accounting Office. rBGH. FDA Approval Should Be Withheld Until the Mastitis Issues is Resolved. 1992.
8. Mepham TB. Public health implications of bovine somatotropin use in dairying: discussion paper. Journal of the Royal Society of Medicine 85:736-739, 1992.
9. Millstone E, et al. Plagiarism or protecting public health? Nature 371:647-648, 1994.
10. U.S. General Accounting Office. Recombinant bovine growth hormone. FDA approval should be withheld until the mastitis issue is resolved. 1992.
11. Davis SR, et al. Effects of injecting growth hormone of thyroxine on milk production and blood plasma concentrations of insulin-like growth factors I and II in dairy cows.
Journal of Endocrinology 114:17-24, 1987.
12. Prosser CG, et al. Changes in concentrations of IGF-1 in milk during BGH treatment in the goat. Journal of Endocrinology 112 (March Supplement): Abstract 65, 1987.
13. McBride BW, et al. The influence of bovine growth hormone (somatotropin) on animals and their products. Research and Development in Agriculture 5:1-21, 1988. page 5
14. Francis GL, et al. Insulin-like growth factors 1 and 2 in bovine colostrum. Sequences and biological activities compared with those of a potent truncated form. Biochem J. 251:95-103, 1988.
15. Prosser CG, et al. Increased secretion of insulin-like growth factor-1 into Milk of cows treated with recombinantly derived bovine growth hormones. Journal of Dairy Research 56:17-26, 1989.
16. Juskevich JC & Guyer CG. Bovine growth hormone food safety evaluation.
Science 249:875-884, 1990.
17. National Institutes of Health. Technology Assessment Conference Statement on
Bovine Somatotropin. Journal of the American Medical Association 265:1423-1425, 1991.
18. Joint FAO/WHO Expert Committee on Food Additives (JECFA). Fortieth Report,
Geneva. June 9-18, 1992. Cited six unpublished industry studies confirming increased IGF-1 levels in rBGH milk. These included one by Monsanto (Schams et al, 1988) reporting a four-fold increase, and another (Miller et al, 1989) reporting a further 50% increase following pasteurization.
19. Epstein SS. BST and cancer. New Scientist U.K., October 29, 1994.
20. Mepham TB, et al. Safety of milk from cows treated with bovine somatotropin.
The Lancet 2:197, 1994
21. Mepham TB & Schofield PN. International Dairy Federation Nutrition Week, Paris, June 1995.
22. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones:
a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
23. Furlanetto RW & DiCarlo JN. Somatotropin-C receptors and growth effects in human breast cells maintained in long-term tissue culture. Cancer Research 44:2122-2128, 1984.
24. Glimm DR, et al. Effect of bovine somatotropin in the distribution of immunoreactive insulin-like growth factor-1 in lactating bovine mammary tissue.
Journal of Dairy Science 71:2923-2935, 1988.
25. Reynolds RK, et al. Regulation of epidermal growth factor and insulin-like growth factors I receptors by estradiol and progesterone in normal and neoplastic endometrial cells cultures. Gynecology Oncology 38:396-406, 1990. page 6
26. Lippman A. Growth factors, receptors and breast cancer. National Institutes of Health Research 3:59-62, 1991.
27. Rosen N, et al. Insulin-like growth factors in human breast cancer. Breast Cancer Research Treatment 18 (Suppl):555-562, 1991.
28. Harris JR, et al. Breast Cancer. New England Journal of Medicine 7:473-480, 1992.
29. Pollak MN, et al. Tamoxifen reduced insulin-like growth factor-1 (IGF-1). Breast Cancer Research Treatment 22:91-100, 1992.
30. Lippman ME. The development of biological therapies for breast cancer. Science 259:631-632, 1993.
31. Pappa V, et al. Insulin-like growth facotr-1 receptors are over expressed and predict a low risk in human breast cancer. Cancer Research 53:3736-3740, 1993.
32. Bruning PF, et al. Insulin-like growth factor-binding protein 3 is decreased in early-stage operable pre-menopausal breast cancer. International Journal of Cancer 62(3):266-270, July 1995.
33. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
34. LeRoith D. Insulin-like growth factors and cancer. Annals of Internal Medicine 122(1):54-59, January, 1995.
35. Bohlke K, et al. Insulin-like growth factor-1 in relation to premenopausal ductal carcinoma in situ of the breast. Epidemiology 9(5):570-573, 1998.
36. Del Giudice ME, et al. Insulin and related factors in premenopausal breast cancer risk. Breast Cancer Research and Treatment 47 (2):111-120, 1998.
37. Hankinson SE, et al. Circulating concentrations of insulin-like growth factor-1 and risk of breast cancer. The Lancet 351:1393-1396, 1998.
38. Agurs-Collins T, et al. Insulin-like growth factor-1 and breast cancer risk in post-menopausal American women. Proceedings of the American Association of Cancer Research 40:152, 1999.
39. Toniolo P, et al. Serum insulin-like growth factor-1 and breast cancer.
International Journal of Cancer 88(5):828-832, 2000.
40. Yu H & Rohan T. Role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 92:1472-1484, 2000. page 7
41. Epstein SS. Re Role of the insulin-like growth factors in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001.
42. Pines A, et al. Gastrointestinal tumors in acromegalic patients. Am J Gastroenterology 80:266-269, 1985.
43. Orme SM, et al. Cancer incidence and mortality in acromegaly: a retrospective cohort study. Journal of Endocrinology Supplement Number OC22, June 1996.
44. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
45. Manousos O, et al. IGF-I and IGF-II in relation to colorectal cancer. International Journal of Cancer 83:15-17, 1999.
46. Ma J, et al. Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor-1 and IGF-1 binding protein-3. Journal of the National Cancer Institute 91:620-625, 1999.
47. Giovannucci E, et al. Plasma insulin-like growth factor-I and binding protein-3 and risk of colorectal cancer and adenoma in women. Proceedings of the American Association of Cancer Research 40:211, 1999.
48. Renehan AG, et al. Circulating insulin-like growth factor II and colorectal adenomas. Journal of Clinical Endocrinology & Metabolism 85(9):3402-3408, 2000.
49. Mantzoros CS, et al. Insulin-like growth factor 1 in relation to prostate cancer and benign prostatic hyperplasia. British Journal of Cancer 76:1115-1118, 1997.
50. Chan JM, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 279:563-566, 1998.
51. Wolk A, et al. Insulin-like growth factor 1 and prostate cancer risk: a population-based, case-control study. Journal of the National Cancer Institute 90:911-915, 1998.
52. Signorello LB, et al. Insulin-like growth factor-binding protein-1 and prostate cancer.
Journal of the National Cancer Institute 91:1965-1967, 1999.
53. Stattin P, et al. Plasma insulin-like growth factor-binding proteins, and prostate
cancer risk: a prospective study. Journal of the National Cancer Institute 92:1910-1917, 2000.
54. Harman SM, et al. Serum levels of insulin-like growth factor I (IGF-1), IGF-II, IGF-binding protein-3, and prostate-specific antigen as predictors of clinical prostate cancer.
Journal of Clinical Endocrinology & Metabolism 85(11):4258-4265, 2000. page 8
55. Juul A, et al. The ratio between serum levels of IGF-1 and the IGF binding protein decreases with age in healthy patients and is increased in acromegalic patients. Clinical Endocrinology 41:85-93, 1994.
56. Tremble JM & McGregor AM. In Treating Acromegaly, editor Wass p. 5-12.
Journal of Endocrinology Ltd., Bristol, England, 1994.
57. Resnicoff M, et al. The insulin-like growth factor-I receptor protects tumor cells from apoptosis in vivo. Cancer Research 55(11):2463-2469, June 1,1995.
58. Epstein SS. Re: role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001
59. Milk Pricing in the United States. By Alden C. Manchester and Don P. Blayney.
Market and Trade Economics Division, Economic Research Service, U.S. Department
of Agriculture. Agriculture Information Bulletin No. 761.
60. Pennington JAT. Bowes and Churches Food Values of Portions Commonly Used, 17th ed. New York: Lippincott, 1998.
61. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.
62. Cramer DW, Harlow BL, Willet WC. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
63. Outwater JL, Nicholson A, Barnard N. Dairy products and breast cancer: the IGF-1, estrogen, and bGH hypothesis. Medical Hypothesis 1997;48:453-61.
64. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-1 and prostate cancer risk: a prospective study. Science 1998;279:563-5.
65. World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute of Cancer Research. Washington, D.C.: 1997.
66. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ1997;315:1255-69.
67. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr 1990;51:489-91.
68. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.
69. Feskanich D, Willet WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Public Health 1997;87:992-7.
70. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994;139:493-505.
71. Huang Z, Himes JH, McGovern PG. Nutrition and subsequent hip fracture risk among a national cohort of white women. Am J Epidemiol 1996;144:124-34.
72. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.
73. Finn SC. The skeleton crew: is calcium enough? J Women’s Health 1998;7(1):31-6.
74. Nordin CBE. Calcium and osteoporosis. Nutrition 1997;3(7/8):664-86.
75. Reid DM, New SA. Nutritional influences on bone mass. Proceed Nutr Soc 1997;56:977-87.
76. Tucker KL, Hannan MR, Chen H, Cupples LA, Wilson PWF, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36.
77. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone mineral density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.
78. The Cornell-China-Oxford Project. The China Study- Dr. T .Colin Campbell 2006
The industry wide shockwaves expected will assist in bringing US production regulations closer to that of our trading partners. In Europe and Canada US dairy exports recently have faced increasing resistance because of the refusal by American producers to discontinue using the hormone. European and Canadian authorities banned the hormone, recognize RBST as a threat to human health and have linked it to cancer. Several years ago documents came to public attention that showed Monsanto lied about their studies in order to gain approval from the FDA. The evidence on this is stunning and I have included an exhaustive list of references and hope that everyone gives them at least a quick glance.[1-58]
The good news for the consumers and the cows is not in any case good news for Monsanto, they are going to lose billions of dollars. Monsanto is the only supplier of the hormone, sold under the name Posilac, and sales have been estimated at close to $300 million annually, although Monsanto refuses disclosure of actual figures. Monsanto Corporation, in case anyone has forgotten, is that esteemed member of the American corporate community that has brought us such wonders as Agent Orange, Roundup and is the world's leader in GMO's (genetically modified organism).
RBST or Posilac is also an excellent example of corporate welfare. Posilac causes cows to produce more milk. So... what is wrong with that you ask? American taxpayers pay farmers not to produce milk and have been doing so for years. [59] There is an excess of dairy products in this country and our government buys it using our money. They buy it to keep the prices stable. If the supply exceeds demand, the price of dairy drops. The government steps in and keeps product from reaching the market. It ends up in government warehouses where much of it is simply thrown away. This is where “government cheese” came from. What is not eaten by our poor, elderly, and native populations ends up in the trash. Do you think that Monsanto cares about the fact that their product is contributing to this? I think Monsanto sees the bottom line.
The trouble with this continues because not only has Posilac been recognized as a human health threat, but so is the milk it helps produce more of! Dairy proteins and fats have been linked to heart disease, stroke [60,6], cancer [62-66], diabetes (types 1&2) [67,68], multiple sclerosis, arthritis, Crohn’s disease, irritable bowl syndrome, fibromyalgia, osteoporosis [69-78], and more. So where did Monsanto get the bright idea for such a great product? Since great minds think alike, maybe it was a friend of one of Monsanto’s other top executives; Donald Rumsfeld was a CEO for Monsanto. Hmmmm.
My hat is off to the California dairy producers for standing up to Monsanto and their money grubbing schemes regardless of the reason. It is a rare day when I have anything positive to say about the dairy industry, today just happens to be one of them.
References
1. Conyers, John. Letter to Richard R. Kusserow, Inspector General, Department of
Health and Human Services. May 9, 1990.
2. Kennelly J & DeBoer G. Bovine somatotropin. In Proceedings of the Alberta Dairy Seminar. Banff, Alberta, March 9-11, 1998.
3. Baer RJ, et al. Composition and flavor of milk produced by cows injected with recombinant bovine somatotropin. Journal of Dairy Science 72:1424-1434, 1989.
4. Capuco, AV et al. Somatotropin increases thyroxine-5’-monodeiodinase activity in lactating mammary tissue of the cow. Journal of Endocrinology 121(2):205-211, 1989.
5. Epstein, SS. Potential public health hazards of biosynthetic milk hormones.
International Journal of Health Services 20:73-84, 1990.
6. Kronfeld, DS. Safety of bovine growth hormone. Science 251:256-257, 1991.
7. U.S. General Accounting Office. rBGH. FDA Approval Should Be Withheld Until the Mastitis Issues is Resolved. 1992.
8. Mepham TB. Public health implications of bovine somatotropin use in dairying: discussion paper. Journal of the Royal Society of Medicine 85:736-739, 1992.
9. Millstone E, et al. Plagiarism or protecting public health? Nature 371:647-648, 1994.
10. U.S. General Accounting Office. Recombinant bovine growth hormone. FDA approval should be withheld until the mastitis issue is resolved. 1992.
11. Davis SR, et al. Effects of injecting growth hormone of thyroxine on milk production and blood plasma concentrations of insulin-like growth factors I and II in dairy cows.
Journal of Endocrinology 114:17-24, 1987.
12. Prosser CG, et al. Changes in concentrations of IGF-1 in milk during BGH treatment in the goat. Journal of Endocrinology 112 (March Supplement): Abstract 65, 1987.
13. McBride BW, et al. The influence of bovine growth hormone (somatotropin) on animals and their products. Research and Development in Agriculture 5:1-21, 1988. page 5
14. Francis GL, et al. Insulin-like growth factors 1 and 2 in bovine colostrum. Sequences and biological activities compared with those of a potent truncated form. Biochem J. 251:95-103, 1988.
15. Prosser CG, et al. Increased secretion of insulin-like growth factor-1 into Milk of cows treated with recombinantly derived bovine growth hormones. Journal of Dairy Research 56:17-26, 1989.
16. Juskevich JC & Guyer CG. Bovine growth hormone food safety evaluation.
Science 249:875-884, 1990.
17. National Institutes of Health. Technology Assessment Conference Statement on
Bovine Somatotropin. Journal of the American Medical Association 265:1423-1425, 1991.
18. Joint FAO/WHO Expert Committee on Food Additives (JECFA). Fortieth Report,
Geneva. June 9-18, 1992. Cited six unpublished industry studies confirming increased IGF-1 levels in rBGH milk. These included one by Monsanto (Schams et al, 1988) reporting a four-fold increase, and another (Miller et al, 1989) reporting a further 50% increase following pasteurization.
19. Epstein SS. BST and cancer. New Scientist U.K., October 29, 1994.
20. Mepham TB, et al. Safety of milk from cows treated with bovine somatotropin.
The Lancet 2:197, 1994
21. Mepham TB & Schofield PN. International Dairy Federation Nutrition Week, Paris, June 1995.
22. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones:
a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
23. Furlanetto RW & DiCarlo JN. Somatotropin-C receptors and growth effects in human breast cells maintained in long-term tissue culture. Cancer Research 44:2122-2128, 1984.
24. Glimm DR, et al. Effect of bovine somatotropin in the distribution of immunoreactive insulin-like growth factor-1 in lactating bovine mammary tissue.
Journal of Dairy Science 71:2923-2935, 1988.
25. Reynolds RK, et al. Regulation of epidermal growth factor and insulin-like growth factors I receptors by estradiol and progesterone in normal and neoplastic endometrial cells cultures. Gynecology Oncology 38:396-406, 1990. page 6
26. Lippman A. Growth factors, receptors and breast cancer. National Institutes of Health Research 3:59-62, 1991.
27. Rosen N, et al. Insulin-like growth factors in human breast cancer. Breast Cancer Research Treatment 18 (Suppl):555-562, 1991.
28. Harris JR, et al. Breast Cancer. New England Journal of Medicine 7:473-480, 1992.
29. Pollak MN, et al. Tamoxifen reduced insulin-like growth factor-1 (IGF-1). Breast Cancer Research Treatment 22:91-100, 1992.
30. Lippman ME. The development of biological therapies for breast cancer. Science 259:631-632, 1993.
31. Pappa V, et al. Insulin-like growth facotr-1 receptors are over expressed and predict a low risk in human breast cancer. Cancer Research 53:3736-3740, 1993.
32. Bruning PF, et al. Insulin-like growth factor-binding protein 3 is decreased in early-stage operable pre-menopausal breast cancer. International Journal of Cancer 62(3):266-270, July 1995.
33. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
34. LeRoith D. Insulin-like growth factors and cancer. Annals of Internal Medicine 122(1):54-59, January, 1995.
35. Bohlke K, et al. Insulin-like growth factor-1 in relation to premenopausal ductal carcinoma in situ of the breast. Epidemiology 9(5):570-573, 1998.
36. Del Giudice ME, et al. Insulin and related factors in premenopausal breast cancer risk. Breast Cancer Research and Treatment 47 (2):111-120, 1998.
37. Hankinson SE, et al. Circulating concentrations of insulin-like growth factor-1 and risk of breast cancer. The Lancet 351:1393-1396, 1998.
38. Agurs-Collins T, et al. Insulin-like growth factor-1 and breast cancer risk in post-menopausal American women. Proceedings of the American Association of Cancer Research 40:152, 1999.
39. Toniolo P, et al. Serum insulin-like growth factor-1 and breast cancer.
International Journal of Cancer 88(5):828-832, 2000.
40. Yu H & Rohan T. Role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 92:1472-1484, 2000. page 7
41. Epstein SS. Re Role of the insulin-like growth factors in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001.
42. Pines A, et al. Gastrointestinal tumors in acromegalic patients. Am J Gastroenterology 80:266-269, 1985.
43. Orme SM, et al. Cancer incidence and mortality in acromegaly: a retrospective cohort study. Journal of Endocrinology Supplement Number OC22, June 1996.
44. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
45. Manousos O, et al. IGF-I and IGF-II in relation to colorectal cancer. International Journal of Cancer 83:15-17, 1999.
46. Ma J, et al. Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor-1 and IGF-1 binding protein-3. Journal of the National Cancer Institute 91:620-625, 1999.
47. Giovannucci E, et al. Plasma insulin-like growth factor-I and binding protein-3 and risk of colorectal cancer and adenoma in women. Proceedings of the American Association of Cancer Research 40:211, 1999.
48. Renehan AG, et al. Circulating insulin-like growth factor II and colorectal adenomas. Journal of Clinical Endocrinology & Metabolism 85(9):3402-3408, 2000.
49. Mantzoros CS, et al. Insulin-like growth factor 1 in relation to prostate cancer and benign prostatic hyperplasia. British Journal of Cancer 76:1115-1118, 1997.
50. Chan JM, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 279:563-566, 1998.
51. Wolk A, et al. Insulin-like growth factor 1 and prostate cancer risk: a population-based, case-control study. Journal of the National Cancer Institute 90:911-915, 1998.
52. Signorello LB, et al. Insulin-like growth factor-binding protein-1 and prostate cancer.
Journal of the National Cancer Institute 91:1965-1967, 1999.
53. Stattin P, et al. Plasma insulin-like growth factor-binding proteins, and prostate
cancer risk: a prospective study. Journal of the National Cancer Institute 92:1910-1917, 2000.
54. Harman SM, et al. Serum levels of insulin-like growth factor I (IGF-1), IGF-II, IGF-binding protein-3, and prostate-specific antigen as predictors of clinical prostate cancer.
Journal of Clinical Endocrinology & Metabolism 85(11):4258-4265, 2000. page 8
55. Juul A, et al. The ratio between serum levels of IGF-1 and the IGF binding protein decreases with age in healthy patients and is increased in acromegalic patients. Clinical Endocrinology 41:85-93, 1994.
56. Tremble JM & McGregor AM. In Treating Acromegaly, editor Wass p. 5-12.
Journal of Endocrinology Ltd., Bristol, England, 1994.
57. Resnicoff M, et al. The insulin-like growth factor-I receptor protects tumor cells from apoptosis in vivo. Cancer Research 55(11):2463-2469, June 1,1995.
58. Epstein SS. Re: role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001
59. Milk Pricing in the United States. By Alden C. Manchester and Don P. Blayney.
Market and Trade Economics Division, Economic Research Service, U.S. Department
of Agriculture. Agriculture Information Bulletin No. 761.
60. Pennington JAT. Bowes and Churches Food Values of Portions Commonly Used, 17th ed. New York: Lippincott, 1998.
61. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.
62. Cramer DW, Harlow BL, Willet WC. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
63. Outwater JL, Nicholson A, Barnard N. Dairy products and breast cancer: the IGF-1, estrogen, and bGH hypothesis. Medical Hypothesis 1997;48:453-61.
64. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-1 and prostate cancer risk: a prospective study. Science 1998;279:563-5.
65. World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute of Cancer Research. Washington, D.C.: 1997.
66. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ1997;315:1255-69.
67. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr 1990;51:489-91.
68. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.
69. Feskanich D, Willet WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Public Health 1997;87:992-7.
70. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994;139:493-505.
71. Huang Z, Himes JH, McGovern PG. Nutrition and subsequent hip fracture risk among a national cohort of white women. Am J Epidemiol 1996;144:124-34.
72. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.
73. Finn SC. The skeleton crew: is calcium enough? J Women’s Health 1998;7(1):31-6.
74. Nordin CBE. Calcium and osteoporosis. Nutrition 1997;3(7/8):664-86.
75. Reid DM, New SA. Nutritional influences on bone mass. Proceed Nutr Soc 1997;56:977-87.
76. Tucker KL, Hannan MR, Chen H, Cupples LA, Wilson PWF, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36.
77. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone mineral density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.
78. The Cornell-China-Oxford Project. The China Study- Dr. T .Colin Campbell 2006
Tuesday, March 6, 2007
Arsenic Levels High in Chickens
Arsenic in Chicken
After reviewing 5000 chicken samples, researchers from the National Institutes of Health and the USDA's Food Safety Inspection Service recently reported alarmingly high levels of arsenic contamination in the flesh of broiler chickens[1] These government researchers found that the amount of arsenic in chicken greatly exceeded the Environmental Protection Agency's new upper safety limit of arsenic allowed in drinking water. In fact, the amount of arsenic found in chicken was 6 to 9 times that allowed by the EPA. A "bucket" of Kentucky Fried Chicken would be expected to have up to almost fifty times the amount of arsenic allowed in a glass of water.[2]
How did the arsenic get into the chickens? The poultry industry fed it to them. Most broiler chickens (which constitute 99% of the chicken meat that people eat) are fed arsenic in the United States[3,4] Although fish and shellfish also present significant dietary sources of arsenic,[6] according to the Food and Drug Administration arsenic compounds are extensively added to the feed of animals--particularly chickens and pigs--to make them grow faster.[5] The animals Americans eat are so heavily infested with internal parasites that adding arsenic to the feed can result in a "stunning" increase in growth rates.[7]
Dr. Ellen Silbergeld, a researcher from the Johns Hopkins School of Public Health, said the poultry industry's practice of using arsenic compounds in its feed is something that has not been studied. "It's an issue everybody is trying to pretend doesn't exist," she said.[8] "Arsenic acted as a growth stimulant in chickens -- develops the meat faster -- and since then, the poultry industry has gone wild using this ingredient," says Donald Herman, a Mississippi agricultural consultant and former Environmental Protection Agency researcher who has studied this use of arsenic for a decade. "And they've tried everything to refrain it from becoming public knowledge,".[9]
The poultry industry argues that the organic form of arsenic given to chickens isn't toxic.[10] "This study appears to be much ado about nothing," says Richard Lobb, the public relations Director of the National Chicken Council. He says the less toxic form of arsenic is "used responsibly and safely by poultry producers."[11] The researchers, however, found not only elevated levels of organic arsenic in chicken meat, they found elevated levels of the highly toxic inorganic form typically used only in insecticides and weed killers.[12] And cooking the muscles of these animals may create additional toxic arsenic by-products.[13]
Inorganic arsenic is considered one of the prominent environmental causes of cancer mortality in the world.[14] Arsenic is a human carcinogen linked to liver, lung, skin, kidney, bladder and prostate cancers. It can also cause neurological, cardiovascular, gastrointestinal and immune system abnormalities. Diabetes has also been linked to arsenic exposure.[15]
The feeding of arsenic to chickens in the U.S. releases hundreds of tons of arsenic into the environment every year in the form of poultry manure which is spread on fields as fertilizer.[16] In fact there's currently a coalition of families suffering serious health conditions suing chicken producers like Tyson after research showed cancer rates as much as 50 times above the national average in communities neighboring factory farmed poultry operations.
The February 2004 Medical Letter on the CDC & FDA concludes "Chicken consumption may contribute significant amounts of arsenic to total arsenic exposure of the U.S. population..." Levels of arsenic in chicken are so high that other sources may have to be monitored carefully to prevent undue toxic exposure among the population.[17]
1 Environmental Health Perspectives 112(2004):18.
2 One KFC bucket contains 3 legs, 3 breasts, 3 wings and 3 thighs [http://cspinet.org/new/pdf/letter_to_ftc.pdf] weighing a total of 1176 grams [http://www.yum.com/nutrition/documents/kfc_nutrition.pdf] containing up to 108.5 mcg of inorganic arsenic [Environmental Health Perspectives 112(2004):18] exceeding to EPA limit on an 8oz. glass of water by a factor of 48.4 [EPA 815- Z- 01- 001].
3 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
4 Medical Letter on the CDC & FDA February 1, 2004
5 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
6 Ibid.
7 Texas Lawyer, January 23, 1995
8 Daily Times (Salisbury, MD) January 4, 2004
9 Texas Lawyer, January 23, 1995
10 Daily Times (Maryland) 11 January 2004.
11 Health Day News 19 January 2004.
12 Environmental Health Perspectives 112(2004):18.
13 Hanaoka, K., Goessler, W., Ohno, H., Irgolic, K. J., and Kaise, T., (2001). Formation of toxic arsenical in roasted muscles of marine animals, Appl. Organometal. Chem., 15: 61- 66.
14 Smith, A.H., C. Hopenhayn-Rich, M.L. Bates, H.M. Goeden, I. HertzPicciotto, H.M. Duggan, R. Wood, M.J. Kosnett, and M.T. Smith. 1992. Cancer risks from arsenic in drinking water. Environmental Health Perspectives 97, 259-267.
15 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
16 Ibid.
17 Medical Letter on the CDC & FDA February 1, 2004
After reviewing 5000 chicken samples, researchers from the National Institutes of Health and the USDA's Food Safety Inspection Service recently reported alarmingly high levels of arsenic contamination in the flesh of broiler chickens[1] These government researchers found that the amount of arsenic in chicken greatly exceeded the Environmental Protection Agency's new upper safety limit of arsenic allowed in drinking water. In fact, the amount of arsenic found in chicken was 6 to 9 times that allowed by the EPA. A "bucket" of Kentucky Fried Chicken would be expected to have up to almost fifty times the amount of arsenic allowed in a glass of water.[2]
How did the arsenic get into the chickens? The poultry industry fed it to them. Most broiler chickens (which constitute 99% of the chicken meat that people eat) are fed arsenic in the United States[3,4] Although fish and shellfish also present significant dietary sources of arsenic,[6] according to the Food and Drug Administration arsenic compounds are extensively added to the feed of animals--particularly chickens and pigs--to make them grow faster.[5] The animals Americans eat are so heavily infested with internal parasites that adding arsenic to the feed can result in a "stunning" increase in growth rates.[7]
Dr. Ellen Silbergeld, a researcher from the Johns Hopkins School of Public Health, said the poultry industry's practice of using arsenic compounds in its feed is something that has not been studied. "It's an issue everybody is trying to pretend doesn't exist," she said.[8] "Arsenic acted as a growth stimulant in chickens -- develops the meat faster -- and since then, the poultry industry has gone wild using this ingredient," says Donald Herman, a Mississippi agricultural consultant and former Environmental Protection Agency researcher who has studied this use of arsenic for a decade. "And they've tried everything to refrain it from becoming public knowledge,".[9]
The poultry industry argues that the organic form of arsenic given to chickens isn't toxic.[10] "This study appears to be much ado about nothing," says Richard Lobb, the public relations Director of the National Chicken Council. He says the less toxic form of arsenic is "used responsibly and safely by poultry producers."[11] The researchers, however, found not only elevated levels of organic arsenic in chicken meat, they found elevated levels of the highly toxic inorganic form typically used only in insecticides and weed killers.[12] And cooking the muscles of these animals may create additional toxic arsenic by-products.[13]
Inorganic arsenic is considered one of the prominent environmental causes of cancer mortality in the world.[14] Arsenic is a human carcinogen linked to liver, lung, skin, kidney, bladder and prostate cancers. It can also cause neurological, cardiovascular, gastrointestinal and immune system abnormalities. Diabetes has also been linked to arsenic exposure.[15]
The feeding of arsenic to chickens in the U.S. releases hundreds of tons of arsenic into the environment every year in the form of poultry manure which is spread on fields as fertilizer.[16] In fact there's currently a coalition of families suffering serious health conditions suing chicken producers like Tyson after research showed cancer rates as much as 50 times above the national average in communities neighboring factory farmed poultry operations.
The February 2004 Medical Letter on the CDC & FDA concludes "Chicken consumption may contribute significant amounts of arsenic to total arsenic exposure of the U.S. population..." Levels of arsenic in chicken are so high that other sources may have to be monitored carefully to prevent undue toxic exposure among the population.[17]
1 Environmental Health Perspectives 112(2004):18.
2 One KFC bucket contains 3 legs, 3 breasts, 3 wings and 3 thighs [http://cspinet.org/new/pdf/letter_to_ftc.pdf] weighing a total of 1176 grams [http://www.yum.com/nutrition/documents/kfc_nutrition.pdf] containing up to 108.5 mcg of inorganic arsenic [Environmental Health Perspectives 112(2004):18] exceeding to EPA limit on an 8oz. glass of water by a factor of 48.4 [EPA 815- Z- 01- 001].
3 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
4 Medical Letter on the CDC & FDA February 1, 2004
5 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
6 Ibid.
7 Texas Lawyer, January 23, 1995
8 Daily Times (Salisbury, MD) January 4, 2004
9 Texas Lawyer, January 23, 1995
10 Daily Times (Maryland) 11 January 2004.
11 Health Day News 19 January 2004.
12 Environmental Health Perspectives 112(2004):18.
13 Hanaoka, K., Goessler, W., Ohno, H., Irgolic, K. J., and Kaise, T., (2001). Formation of toxic arsenical in roasted muscles of marine animals, Appl. Organometal. Chem., 15: 61- 66.
14 Smith, A.H., C. Hopenhayn-Rich, M.L. Bates, H.M. Goeden, I. HertzPicciotto, H.M. Duggan, R. Wood, M.J. Kosnett, and M.T. Smith. 1992. Cancer risks from arsenic in drinking water. Environmental Health Perspectives 97, 259-267.
15 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
16 Ibid.
17 Medical Letter on the CDC & FDA February 1, 2004
A penny's worth of cinnamon a day Lowers Cholesterol as Well as Drugs and Improves Blood Sugar Control
Cinnamon: Spice Up Your Life
Most of us remember the blueberry story that soaked the press several years ago describing the antioxidant power of the berry's blue pigment. The anti-cancer properties of blueberries literally... come out of the blue. Whether we were talking about the orange beta carotene in sweet potatoes, or the red lycopene in tomatoes, the colors themselves are the antioxidants.
The blueberry study tested only 40 fruits and vegetables, though. Newer data shows that blueberries, the previous "number one" antioxidant food, got their little blue butts kicked down to number six. Just when we thought blueberries were the winners, someone tested walnuts, which then took the lead. And now, just when walnuts were getting cocky, someone looked at herbs and spices, which almost all blow walnuts out of the water. We now know that lots of the flavor compounds in herbs are powerful antioxidants as well. The flavors are the antioxidants. So there's these compounds called gingerols. Guess where they're found? Don't forget rosmarinic acid... So for maximum nutrition we should eat colorful and flavorful foods.
On a per weight basis herbs and spices rule the plant kingdom, but how many grams of cloves can people eat? And just because herbs and spices are at the top of the antioxidant ladder doesn't necessarily translate into clinical benefit. While U.S. scientists continued to tinker our tax dollars away force-feeding rodents blueberry pulp, researchers in Pakistan had the novel idea of actually studying human beings.
Researchers took 30 men and 30 women--all with type II diabetes--and gave half of them capsules containing cinnamon and half of them placebo capsules. After 40 days, those eating just 1/4 teaspoon of cinnamon a day not only had significantly better blood sugar control, but their cholesterol dropped almost 30%--that's like what you see in cholesterol-lowering drugs!
Why hasn't this study been plastered all over the front pages? It was certainly published in a prestigious American medical journal. Perhaps it's because, although the statin medications net drug companies billions in profit every year, a 1/4 teaspoon of cinnamon costs me less than a penny a day in the bulk bin at my local co-op. And the research suggests that even just a pinch a day (less than 1/8 teaspoon) might have a similar effect.[6]. Are other spices as medicinal as cinnamon? I guess we'll just have to wait for the government of Pakistan to fund more studies.
[6] Diabetes Care 26(12):3215.
Most of us remember the blueberry story that soaked the press several years ago describing the antioxidant power of the berry's blue pigment. The anti-cancer properties of blueberries literally... come out of the blue. Whether we were talking about the orange beta carotene in sweet potatoes, or the red lycopene in tomatoes, the colors themselves are the antioxidants.
The blueberry study tested only 40 fruits and vegetables, though. Newer data shows that blueberries, the previous "number one" antioxidant food, got their little blue butts kicked down to number six. Just when we thought blueberries were the winners, someone tested walnuts, which then took the lead. And now, just when walnuts were getting cocky, someone looked at herbs and spices, which almost all blow walnuts out of the water. We now know that lots of the flavor compounds in herbs are powerful antioxidants as well. The flavors are the antioxidants. So there's these compounds called gingerols. Guess where they're found? Don't forget rosmarinic acid... So for maximum nutrition we should eat colorful and flavorful foods.
On a per weight basis herbs and spices rule the plant kingdom, but how many grams of cloves can people eat? And just because herbs and spices are at the top of the antioxidant ladder doesn't necessarily translate into clinical benefit. While U.S. scientists continued to tinker our tax dollars away force-feeding rodents blueberry pulp, researchers in Pakistan had the novel idea of actually studying human beings.
Researchers took 30 men and 30 women--all with type II diabetes--and gave half of them capsules containing cinnamon and half of them placebo capsules. After 40 days, those eating just 1/4 teaspoon of cinnamon a day not only had significantly better blood sugar control, but their cholesterol dropped almost 30%--that's like what you see in cholesterol-lowering drugs!
Why hasn't this study been plastered all over the front pages? It was certainly published in a prestigious American medical journal. Perhaps it's because, although the statin medications net drug companies billions in profit every year, a 1/4 teaspoon of cinnamon costs me less than a penny a day in the bulk bin at my local co-op. And the research suggests that even just a pinch a day (less than 1/8 teaspoon) might have a similar effect.[6]. Are other spices as medicinal as cinnamon? I guess we'll just have to wait for the government of Pakistan to fund more studies.
[6] Diabetes Care 26(12):3215.
Dairy Proteins Linked to Multiple Sclerosis
Milk and Multiple Sclerosis
Multiple sclerosis is a devastating disease characterized by your immune system attacking the insulation of your own nerve cells, causing unpredictable short-circuiting within your nervous system, which commonly interferes with vision, speech and mobility.
But why would your immune system do such a thing? We know that other diseases of so-called immune "autoaggression" may be caused by something called "molecular mimicry," in which a foreign protein looks just like one of the body's own proteins. So then when the body makes antibodies against the foreign invader, it also unintentionally makes antibodies against some of the body's own proteins.
For example, there is a protein in bovine milk that looks like a protein in the human pancreas, and so human babies exposed to the milk of cows may try to fend off the foreign bovine protein and, in doing so, destroy their pancreas's ability to produce insulin, leading to type I diabetes.
Numerous population-based studies around the world have linked multiple sclerosis to dairy product consumption,[1-3] but cause and effect could never be proven. So a prestigious research team of German, Swedish, British and American scientists set out study bovine milk proteins and see if they could find any milk protein that cross-reacted with human nerve-sheath proteins. And for the first time ever, they found it.[4]
If a milk protein is causing or contributing to multiple sclerosis, why don't more people come down with the disease? Like all diseases, susceptibility has both a genetic and an environmental component. We don't know why in some people the bovine milk protein is able to sneak through the blood-brain barrier into the central nervous system and potentially trigger an inflammatory response that ends with your own nerves as victims of collateral damage.
This research is still in the preliminary stage, and blaming dairy for multiple sclerosis remains speculative, but evidence is mounting that this disabling disease may just be yet another problem inherent to humans eating the bodies and body fluids of fellow mammals.
[1] Medical hypotheses 19(1986):169.
[2] Neuroepidemiology 11(1992):304.
[3] Annals of Neurology 49(1997):55.
[4] Journal of Immunology 172(2004):661.
Multiple sclerosis is a devastating disease characterized by your immune system attacking the insulation of your own nerve cells, causing unpredictable short-circuiting within your nervous system, which commonly interferes with vision, speech and mobility.
But why would your immune system do such a thing? We know that other diseases of so-called immune "autoaggression" may be caused by something called "molecular mimicry," in which a foreign protein looks just like one of the body's own proteins. So then when the body makes antibodies against the foreign invader, it also unintentionally makes antibodies against some of the body's own proteins.
For example, there is a protein in bovine milk that looks like a protein in the human pancreas, and so human babies exposed to the milk of cows may try to fend off the foreign bovine protein and, in doing so, destroy their pancreas's ability to produce insulin, leading to type I diabetes.
Numerous population-based studies around the world have linked multiple sclerosis to dairy product consumption,[1-3] but cause and effect could never be proven. So a prestigious research team of German, Swedish, British and American scientists set out study bovine milk proteins and see if they could find any milk protein that cross-reacted with human nerve-sheath proteins. And for the first time ever, they found it.[4]
If a milk protein is causing or contributing to multiple sclerosis, why don't more people come down with the disease? Like all diseases, susceptibility has both a genetic and an environmental component. We don't know why in some people the bovine milk protein is able to sneak through the blood-brain barrier into the central nervous system and potentially trigger an inflammatory response that ends with your own nerves as victims of collateral damage.
This research is still in the preliminary stage, and blaming dairy for multiple sclerosis remains speculative, but evidence is mounting that this disabling disease may just be yet another problem inherent to humans eating the bodies and body fluids of fellow mammals.
[1] Medical hypotheses 19(1986):169.
[2] Neuroepidemiology 11(1992):304.
[3] Annals of Neurology 49(1997):55.
[4] Journal of Immunology 172(2004):661.
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